Cardiomyopathies ; diagnosis ; etiology ; therapy ; Humans

Most patients with liver cirrhosis have hyperdynamic circulatory alterations with increased cardiac output, and decreased systemic vascular resistance and arterial pressure. But, in spite of the increased resting cardiac output, ventricular contractile response to stressful stimuli is attenuated in cirrhotic patients which is termed as cirrhotic cardiomyopathy. The prevalence of cirrhotic cardiomyopathy remains unknown at present. Clinical features include structural, histological, electrophysiological, systolic and diastolic dysfunction. Multiple factors are considered as responsible, including impaired beta-adrenergic receptor signal transduction, abnormal membrane biophysical characteristics, and increased activity of cardiodepressant systems mediated by cGMP. Generally, cirrhotic cardiomyopathy with overt severe heart failure is rare. However, major stresses on the cardiovascular system such as liver transplantation, infections and insertion of transjugular intrahepatic portosystemic shunts (TIPS) can unmask the presence of cirrhotic cardiomyopathy and thereby convert latent to overt heart failure. Cirrhotic cardiomyopathy may also contribute to the pathogenesis of hepatorenal syndrome and circulatory failure in liver cirrhosis. Because of the marked paucity of treatment studies, current recommendations for management are empirical, nonspecific measures. Further studies for pathogenesis and new therapeutic strategies in this area are required.
Cardiomyopathies/*diagnosis/*etiology/therapy ; Humans ; Liver Cirrhosis/*complications ; Prognosis

Ventricular premature complexes (VPCs) are known to be one of the most benign cardiac arrhythmias when they occur in structurally normal hearts. We experienced a 32-year old man who presented with dyspnea, palpitations and very frequent VPCs (31% of the total heart beats). Echocardiography revealed a dilated left ventricle (LV 66 mm at end-diastole and 57 mm at end-systole) and a decreased ejection fraction (34%). Very frequent VPCs had been detected 10 years previously and he underwent a failed radiofrequency catheter ablation (RFCA) procedure at that time. The patient had been treated with heart failure medications including betablockers, ACE inhibitors and spironolactone for the two most recent years. Six months after we eliminated these VPCs with a second RFCA procedure, the heart returned to normal function and size. Long standing and very frequent VPCs could be the cause of left ventricular dysfunction in a subset of patients who suffer with dilated cardiomyopathy, and RFCA should be the choice of therapy for these patients.
Ventricular Premature Complexes/*complications ; Tachycardia, Ventricular/*etiology/therapy ; Male ; Humans ; *Catheter Ablation ; Cardiomyopathies/*etiology/therapy ; Adult

OBJECTIVE: To investigate the value of maximal rate of left ventricular pressure (dp/dtmax) in evaluating the changes of cardiac function before and after heart rate reduction in patients with sepsis-induced cardiomyopathy (SIC). METHODS: A single-center, prospective randomized controlled study was conducted. Adult patients with sepsis/septic shock admitted to the department of intensive care unit (ICU) of Tianjin Third Central Hospital from April 1, 2020 to February 28, 2022 were enrolled. Speckle tracking echocardiography (STE) and pulse indication continuous cardiac output (PiCCO) monitoring were performed immediately after the completion of the 1 h-Bundle therapy. The patients with heart rate over 100 beats/minutes were selected and randomly divided into esmolol group and regular treatment group, 55 cases in each group. All patients underwent STE and PiCCO monitoring at 6, 24 and 48 hours after admission in ICU and calculated acute physiology and chronic health evaluation II (APACHE II) and sequential organ failure assessment (SOFA). Primary outcome measure: change in dp/dtmax after reducing heart rate by esmolol. Secondary outcome measures: correlation between dp/dtmax and global longitudinal strain (GLS); changes of vasoactive drug dosage, oxygen delivery (DO₂), oxygen consumption (VO₂) and stroke volume (SV) after the administration of esmolol; proportion of heart rate reaching the target after the administration of esmolol; 28-day and 90-day mortality in two groups. RESULTS: Baseline data on age, gender, body mass index, SOFA score, APACHE II score, heart rate, mean arterial pressure, lactic acid, 24-hour fluid balance, sepsis etiology and prior comorbidities were similar between esmolol group and regular treatment group, there were no significant differences between the two groups. All SIC patients achieved the target heart rate after 24 hours of esmolol treatment. Compared with regular treatment group, parameters reflecting myocardial contraction such as GLS, global ejection fraction (GEF) and dp/dtmax were significantly increased in esmolol group [GLS: (-12.55±4.61)% vs. (-10.73±4.82)%, GEF: (27.33±4.62)% vs. (24.18±5.35)%, dp/dtmax (mmHg/s): 1 312.1±312.4 vs. 1 140.9±301.0, all P < 0.05], and N-terminal pro-brain natriuretic peptide (NT-proBNP) significantly decreased [μg/L: 1 364.52 (754.18, 2 389.17) vs. 3 508.85 (1 433.21, 6 988.12), P < 0.05], DO₂ and SV were significantly increased [DO₂ (mL×min^-1×m^-2): 647.69±100.89 vs. 610.31±78.56, SV (mL): 49.97±14.71 vs. 42.79±15.77, both P < 0.05]. The system vascular resistance index (SVRI) in esmolol group was significantly higher than that in regular treatment group (kPa×s×L^-1: 287.71±66.32 vs. 251.17±78.21, P < 0.05), even when the dosage of norepinephrine was similar between the two groups. Pearson correlation analysis showed that dp/dtmax was negatively correlated with GLS in SIC patients at 24 hours and 48 hours after ICU admission (r values were -0.916 and -0.935, respectively, both P < 0.05). Although there was no significant difference in 28-day mortality between esmolol group and regular treatment group [30.9% (17/55) vs. 49.1% (27/55), χ² = 3.788, P = 0.052], the rate of esmolol use in patients who died within 28 days was lower than that in patients who survived [38.6% (17/44) vs. 57.6% (38/66), χ² = 3.788, P = 0.040]. In addition, esmolol has no effect on the 90-day mortality of patients. Logistic regression analysis showed that after adjusting for SOFA score and DO₂ factors, patients who used esmolol had a significantly lower risk of 28-day mortality compared with patients who did not use esmolol [odds ratio (OR) = 2.700, 95% confidence interval (95%CI) was 1.038-7.023, P = 0.042]. CONCLUSIONS dp/dtmax in PiCCO parameter can be used as a bedside indicator to evaluate cardiac function in SIC patients due to its simplicity and ease of operation. Esmolol control of heart rate in SIC patients can improve cardiac function and reduce short-term mortality.
Adult ; Humans ; Prospective Studies ; Ventricular Pressure ; Sepsis/complications* ; Shock, Septic/drug therapy* ; Cardiomyopathies/etiology* ; Prognosis

Anti-Arrhythmia Agents ; therapeutic use ; Cardiomyopathies ; drug therapy ; etiology ; Child, Preschool ; Female ; Humans ; Moricizine ; therapeutic use ; Tachycardia ; complications ; drug therapy ; Treatment Outcome

OBJECTIVETo reveal the roles of Rho kinase (ROCK) in the mechanisms of complications in diabetes by reviewing the correlations between ROCK and related complications in diabetes.

DATA SOURCESThe data used in the present article were mainly from PubMed with relevant English articles published from 1998 to 2010. The search terms were "ROCK" and "diabetes".

STUDY SELECTIONOriginal articles including the roles of ROCK or its inhibitors in diabetic complications and review articles about the biological character of ROCK were selected.

RESULTSThe activity and expression of ROCK were up-regulated in the models of type 1 or type 2 diabetes animals and the cultured cells with concentrations of high glucose, ROCK activation was associated with the development or progression of complications in diabetes. Inhibition of RhoA/ROCK pathway prevented or ameliorated the pathologic changes of diabetic complications, and ROCK has been regarded as a key target for treatment of these complications.

CONCLUSIONRhoA/ROCK signaling plays important roles in the pathogenesis of long-term complications in diabetes and ROCK inhibitors are becoming a promising solution to treatments of complications in diabetes.

Animals ; Cardiomyopathies ; etiology ; Diabetes Complications ; etiology ; therapy ; Humans ; Sexual Dysfunction, Physiological ; etiology ; Signal Transduction ; Urinary Bladder Diseases ; etiology ; rho-Associated Kinases ; antagonists & inhibitors ; chemistry ; physiology ; rhoA GTP-Binding Protein ; antagonists & inhibitors ; chemistry ; physiology

Acute Disease ; Adolescent ; Adult ; Bridged-Ring Compounds ; poisoning ; Cardiomyopathies ; etiology ; therapy ; Creatine Kinase ; blood ; Creatine Kinase, MB Form ; Electrocardiography ; Foodborne Diseases ; blood ; complications ; therapy ; Glutamyl Aminopeptidase ; blood ; Humans ; Isoenzymes ; blood ; Male ; Middle Aged ; Nausea ; etiology ; Seizures ; etiology ; Treatment Outcome

OBJECTIVETo evaluate the effects of creatine phosphate (CP) in the treatment of myocardial damage following neonatal asphyxia.

METHODSMedical databases were searched for a systematic literature review and meta-analysis of randomized and quasi-randomized trials on the treatment of myocardial damage with CP following neonatal asphyxia. The data was analyzed using Review Manager 5.1.

RESULTSSix trials involving 400 patients (CP treatment/control: 202/198) were included in the survey. The meta-analysis indicated that CP treatment for 7 days decreased serum myocardial enzyme levels (CK, CK-MB, LDH, HBDH and cTnI levels). Both the total effective rate (RR: 1.29; 95% CI: 1.12, 1.48) and the significantly effective rate (RR: 1.78; 95% CI: 1.32, 2.41) in the CP treatment group were significantly higher than in the control group. CP treatment reduced the hospitalization period by 4.07 days compared with the control group (95% CI: -5.25, -2.89).

CONCLUSIONSCP treatment appears to be more effective than routine treatment alone for myocardial damage following neonatal asphyxia. It appears to be safe and it can both decrease serum myocardial enzyme levels and shorten the period of hospitalization. However, as the evidence obtained in this study is not robust due to the poor quality of current studies, further studies of high-quality, large-scale trails are needed.

Asphyxia Neonatorum ; complications ; Cardiomyopathies ; drug therapy ; etiology ; Cardiotonic Agents ; therapeutic use ; Humans ; Infant, Newborn ; Length of Stay ; Myocytes, Cardiac ; pathology ; Phosphocreatine ; therapeutic use ; Randomized Controlled Trials as Topic

OBJECTIVETo investigate the protective effect of PPARgamma ligands rosiglitazone on myocardium in diabetic cardiomyopathy of rats.

METHODSThe rat model of diabetes was induced by administration of streptozotocin (STZ) for 6 or 10 weeks. In the treatment group the STZ-induced diabetic rats were treated with rosiglitazone. The left ventricular muscle specimens were taken from treatment and control group; then were examined under transmission electron microscope.

RESULTCardiac myofibrils of diabetic rats in control group were obviously fewer and broken. There were fewer and smaller dissolved mitochondria with incomplete membrane and mixed cristae and karyopyknosis. Myocardium of diabetic rats treated with rosiglitazone was markedly improved although their blood glucose levels were still high.

CONCLUSIONHyperglycemia can cause destruction of myocardial cell structure. Rosiglitazone has protective effect on myocardial cells of diabetic rats, which seems to be independent of blood glucose levels.

Animals ; Cardiomyopathies ; drug therapy ; etiology ; pathology ; Cardiotonic Agents ; therapeutic use ; Diabetes Mellitus, Experimental ; complications ; drug therapy ; Hypoglycemic Agents ; therapeutic use ; Ligands ; Male ; Myocardium ; ultrastructure ; PPAR gamma ; therapeutic use ; Rats ; Rats, Sprague-Dawley ; Thiazolidinediones ; therapeutic use

OBJECTIVECarnitine deficiency has been associated with progressive cardiomyopathy due to compromised energy metabolism. The objective of this study was to investigate clinical features of carnitine deficiency-induced cardiomyopathy and the therapeutic efficacy of L-carnitine administration.

METHODBetween January 2010 and December 2011, filter-paper blood spots were collected from 75 children with cardiomyopathy. Free carnitine and acylcarnitine profiles were measured for each individual by tandem mass spectrometry (MS/MS). For those in whom carnitine deficiency was demonstrated, treatment was begun with L-carnitine at a dose of 150 - 250 mg/(kg·d). Clinical evaluation, including physical examination, electrocardiography, chest x-ray, echocardiography and tandem mass spectrometry, was performed before therapy and during follow-up.

RESULTOf 75 cardiomyopathy patients, the diagnosis of carnitine deficiency was confirmed in 6 patients, which included 1 boy and 5 girls. Their age ranged from 0.75 to 6 years. Free carnitine content was (1.55 ± 0.61) µmol/L (reference range 10 - 60 µmol/L). Left ventricular end-diastolic diameter (LVDd) was (5.04 ± 0.66) cm and left ventricular ejection fraction (LVEF) was (38.5 ± 10.5)%. After 10 - 30 d therapy of L-carnitine, free carnitine content rose to (30.59 ± 15.02) µmol/L (t = 4.79, P < 0.01). LVDd decreased to (4.42 ± 0.67) cm (t = 4.28, P < 0.01) and LVEF increased to (49.1 ± 7.6)% (t = 6.59, P < 0.01). All patients received follow-up evaluations beyond 6 months of treatment. Clinical improvement was dramatic. LVEF returned to normal completely in all the 6 patients. LVDd decreased further in all the 6 patients and returned to normal levels in 3 patients. No clinical signs or symptoms were present in any of the 6 patients. The only complications of therapy had been intermittent diarrhea in 1 patient.

CONCLUSIONTandem mass spectrometry is helpful to diagnose carnitine deficiency and should be performed in all children with cardiomyopathy. L-carnitine has a good therapeutic effect on carnitine deficiency-induced cardiomyopathy.

Adolescent ; Cardiomyopathies ; diagnosis ; drug therapy ; etiology ; Cardiotonic Agents ; administration & dosage ; therapeutic use ; Carnitine ; blood ; deficiency ; therapeutic use ; Child ; Child, Preschool ; Electrocardiography ; Female ; Follow-Up Studies ; Humans ; Infant ; Male ; Retrospective Studies ; Tandem Mass Spectrometry ; Treatment Outcome ; Ventricular Function, Left ; drug effects